【精品文献】麝香保心丸
:麝香保心丸:抑制心肌梗死机制
我国中药复方研究水平又上一个新台阶。国际著名系统生物学杂志Molecular
《分子生物系统》今年笫一期刊登了第二军医大学药学院张卫东教授Biosystems
带领课题组完成的一项研究成果,阐明麝香保心丸对冠心病治疗作用的药理机
制,主要是通过整体调整包括炎症反应、能量代谢以及心肌肥大等通路的代谢过
程,从而抑制心肌梗死的进展。
麝香保心丸是上海和黄药业的拳头产品,临床研究显示其对各型心绞痛均有良好
效果。但由于麝香保心丸是由七味中药组成的复方,所含成分复杂,其作用机制
的阐明一直是困扰着该药实现现代化的关键问题。
第二军医大学药学院研究人员几年来通过采用大鼠心脏冠脉左前降支结扎造心
肌梗死模型,以代谢组学为分析手段和对心肌梗死大鼠尿液的分析,探讨心肌梗
死的分子机制,并从整体上考察麝香保心丸对心肌梗死的治疗效果。数据分析显
示,心肌梗死造模后给予麝香保心丸治疗的大鼠状态明显好转,并且有部分大鼠
的状态能达到正常水平。同时,研究还通过对尿液中鉴定的肌酸等5个生物标志
物完全逆转,体现了麝香保心丸可抑制心肌缺血导致的能量代谢紊乱,提高心肌
能量的利用,增加能量供给,从而减少心肌细胞凋亡,降低心肌梗死程度,起到
治疗心肌梗死的作用。
此外,本研究还证实了麝香保心丸对心肌梗死的治疗是一个动态过程,有时间依
赖性。从第3天起,麝香保心丸给药组大鼠开始起治疗作用;第7天大鼠的状态
更加趋于正常组,麝香保心丸的治疗作用进一步加强;第15天大鼠的整体状态
已经部分和正常组大鼠重合,更加趋于正常状态。
这一研究获得了国家新药创制重大专项、国家自然科学基金、上海市中药现代化
基金的支持。已有成果不仅为全面阐明麝香保心丸治疗心肌梗死作用机制奠定了
基础,更为推进其现代化进程提供了理论依据。
原文出处:
Mol. BioSyst. DOI: 10.1039/C0MB00110D
Potential biomarkers in the urine of myocardial infarction rats: a
metabolomic method and its application Peng Jiang, Weixing Dai, Shikai Yan, Zhongliang Chen, Ruilin Xu, Jianmi
Ding, Li Xiang, Shuping Wang, Runhui Liu and Weidong Zhang
Abstract
A metabolomic method using reversed-phase liquid chromatography/quadrupole time-of-flight mass spectrometry (LC-Q-TOF-MS)
was developed to obtain a systematic view of the development and progression of myocardial infarction (MI). By combining with partial least squares discriminant analysis (PLS-DA), 16 biomarkers in rat urine were identified and eight of them were related to the pathway of energy metabolism. Among the regulated pathways, the citric acid cycle related network was acutely perturbed. The metabolomic results not only supplied a systematic view of the development and progression of MI but also provided the theoretical basis for the prevention or treatment of MI. The developed method was also used to analyze the therapeutic effects of a traditional Chinese medicine (TCM) named Shexiang Baoxin Pill (SBP), a widely used anti-MI medicine in clinics. The results showed that SBP administration could provide satisfactory effects on MI through partially regulating the perturbed pathway of energy metabolism.